2nd Med Surg Exam Key Points

Lewis et al: Medical-Surgical Nursing: Assessment and Management of Clinical Problems, 7th edition

Key Points

Chapter 17: Fluid, Electrolyte, and Acid-Base Imbalances

Body fluids and electrolytes play an important role in homeostasis.

Many diseases and their treatments have the ability to affect fluid and electrolyte balance.

Water is the primary component of the body, accounting for approximately 60% of the body weight in the adult.

The two major fluid compartments in the body are intracellular and extracellular.

The measurement of electrolytes is important to the nurse in evaluating electrolyte balance, as well as in determining the composition of electrolyte preparations.

Osmolality is important because it indicates the water balance of the body.

In the metabolically active cell, there is a constant exchange of substances between the cell and the interstitium, but no net gain or loss of water occurs.

The major colloid in the vascular system contributing to the total osmotic pressure is protein.

The amount and direction of movement between the interstitium and the capillary are determined by the interaction of (1) capillary hydrostatic pressure, (2) plasma oncotic pressure, (3) interstitial hydrostatic pressure, and (4) interstitial oncotic pressure.

If capillary or interstitial pressures are altered, fluid may abnormally shift from one compartment to another, resulting in edema or dehydration.

Fluid is drawn into the plasma space whenever there is an increase in the plasma osmotic or oncotic pressure. This could happen with administration of colloids, dextran, mannitol, or hypertonic solutions.

First spacing describes the normal distribution of fluid in the intracellular fluid (ICF) and extracellular fluid (ECF) compartments. Second spacing refers to an abnormal accumulation of interstitial fluid (i.e., edema). Third spacing occurs when fluid accumulates in a portion of the body from which it is not easily exchanged with the rest of the ECF.

Water balance is maintained via the finely tuned balance of water intake and excretion.

An intact thirst mechanism is important for fluid balance. The patient who cannot recognize or act on the sensation of thirst is at risk for fluid deficit and hyperosmolality.

An increase in plasma osmolality or a decrease in circulating blood volume will stimulate antidiuretic hormone (ADH) secretion. Reduction in the release or action of

Copyright © 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

Key Points

ADH produces diabetes insipidus.

Aldosterone is a mineralocorticoid with potent sodium-retaining and potassium-excreting capability.

The primary organs for regulating fluid and electrolyte balance are the kidneys, lungs, and gastrointestinal tract.

Insensible water loss, which is invisible vaporization from the lungs and skin, assists in regulating body temperature.

With severely impaired renal function, the kidneys cannot maintain fluid and electrolyte balance. This condition results in edema, potassium, and phosphorus retention, acidosis, and other electrolyte imbalances.

Structural changes to the kidney and a decrease in the renal blood flow lead to a decrease in the glomerular filtration rate, decreased creatinine clearance, the loss of the ability to concentrate urine and conserve water, and narrowed limits for the excretion of water, sodium, potassium, and hydrogen ions.

Fluid and electrolyte imbalances are commonly classified as deficits or excesses.

Fluid volume deficit can occur with abnormal loss of body fluids (e.g., diarrhea, fistula drainage, hemorrhage, polyuria), inadequate intake, or a plasma-to-interstitial fluid shift.

The use of 24–hour intake and output records gives valuable information regarding fluid and electrolyte problems.

Monitoring the patient for cardiovascular and neurologic changes is necessary to prevent or detect complications from fluid and electrolyte imbalances.

Accurate daily weights provide the easiest measurement of volume status. Weight changes must be obtained under standardized conditions.

Edema is assessed by pressing with a thumb or forefinger over the edematous area.

The rates of infusion of IV fluid solutions should be carefully monitored.

The goal of treatment in fluid and electrolyte imbalances is to treat the underlying cause.

SODIUM Is the major ECF cation.

An elevated serum sodium may occur with water loss or sodium gain.

Hyponatremia:o Common causes include water excess from inappropriate use of sodium-free

or hypotonic IV fluids.o Symptoms of hyponatremia are related to cellular swelling and are first

manifested in the central nervous system (CNS).

POTASSIUM Is the major ICF cation.


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Factors that cause potassium to move from the ICF to the ECF include acidosis, trauma to cells (as in massive soft tissue damage or in tumor lysis), and exercise.

Hyperkalemiao The most common cause is renal failure. Hyperkalemia is also common with

massive cell destruction (e.g., burn or crush injury, tumor lysis); rapid transfusion of stored, hemolyzed blood; and catabolic states (e.g., severe infections).

o Manifestations of hyperkalemia include cramping leg pain, followed by weakness or paralysis of skeletal muscles.

o All patients with clinically significant hyperkalemia should be monitored electrocardiographically to detect dysrhythmias and to monitor the effects of therapy. Cardiac depolarization is decreased, leading to flattening of the P wave and widening of the QRS wave. Repolarization occurs more rapidly, resulting in shortening of the QT interval and causing the T wave to be narrower and more peaked. Ventricular fibrillation or cardiac standstill may occur.

o The patient experiencing dangerous cardiac dysrhythmias should receive IV calcium gluconate immediately while the potassium is being eliminated and forced into cells.

Hypokalemiao The most common causes are from abnormal losses via either the kidneys or

the gastrointestinal tract. Abnormal losses occur when the patient is diuresing, particularly in the patient with an elevated aldosterone level.

o In the patient with hypokalemia, cardiac changes include impaired repolarization, resulting in a flattening of the T wave and eventually in emergence of a U wave. The incidence of potentially lethal ventricular dysrhythmias is increased in hypokalemia.

o Patients taking digoxin experience increased digoxin toxicity if their serum potassium level is low. Skeletal muscle weakness and paralysis may occur with hypokalemia. Severe hypokalemia can cause weakness or paralysis of respiratory muscles, leading to shallow respirations and respiratory arrest.

o Hypokalemia is treated by giving potassium chloride supplements and increasing dietary intake of potassium.

CALCIUM Hypercalcemia

o About two thirds of cases are caused by hyperparathyroidism and one third are caused by malignancy, especially from breast cancer, lung cancer, and multiple myeloma.

o Manifestations of hypercalcemia include decreased memory, confusion, disorientation, fatigue, muscle weakness, constipation, cardiac dysrhythmias, and renal calculi.

o Treatment of hypercalcemia is promotion of excretion of calcium in urine by administration of a loop diuretic and hydration of the patient with isotonic saline infusions.

Hypocalcemia o Is caused by a decrease in the production of parathyroid hormone. o Hypocalcemia is characterized by increased muscle excitability resulting in

tetany.o A patient who has had neck surgery including thyroidectomy is observed


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carefully for signs of hypocalcemia.

Phosphate The major condition that can lead to hyperphosphatemia is acute or chronic renal

failure.

Hypophosphatemia (low serum phosphate) is seen in the patient who is malnourished or has a malabsorption syndrome.

MAGNESIUM Hypomagnesemia (low serum magnesium level) produces neuromuscular and CNS

hyperirritability.

Hypermagnesemia usually occurs only with an increase in magnesium intake accompanied by renal insufficiency or failure.

ACID-BASE IMBALANCES Patients with diabetes mellitus, chronic obstructive pulmonary disease, and kidney

disease frequently develop acid-base imbalances. Vomiting and diarrhea may cause loss of acids and bases.

The nurse must always consider the possibility of acid-base imbalance in patients with serious illnesses.

The buffer system is the fastest acting system and the primary regulator of acid-base balance.

The lungs help maintain a normal pH by excreting CO2 and water, which are by-products of cellular metabolism.

The three renal mechanisms of acid elimination are secretion of small amounts of free hydrogen into the renal tubule, combination of H+ with ammonia (NH3) to form ammonium (NH4

+), and excretion of weak acids.

Acid-base imbalances are classified as respiratory or metabolic.o Respiratory acidosis (carbonic acid excess) occurs whenever there is

hypoventilation.o Respiratory alkalosis (carbonic acid deficit) occurs whenever there is

hyperventilation.o Metabolic acidosis (base bicarbonate deficit) occurs when an acid other

than carbonic acid accumulates in the body or when bicarbonate is lost from body fluids.

o Metabolic alkalosis (base bicarbonate excess) occurs when a loss of acid (prolonged vomiting or gastric suction) or a gain in bicarbonate occurs.

Arterial blood gas (ABG) values provide valuable information about a patient’s acid-base status, the underlying cause of the imbalance, the body’s ability to regulate pH, and the patient’s overall oxygen status.

In cases of acid-base imbalances, the treatment is directed toward correction of the underlying cause.

Fluid replacement therapy is used to correct fluid and electrolyte imbalances.


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o A hypotonic solution provides more water than electrolytes, diluting the ECF. o Plasma expanders stay in the vascular space and increase the osmotic

pressure.o A hypertonic solution initially raises the osmolality by the ECF and expands

it.


Key Points

Chapter 47: Nursing Management: Acute Renal Failure and Chronic Kidney Disease

Renal failure is the partial or complete impairment of kidney function resulting in an inability to excrete metabolic waste products and water.

Renal failure causes functional disturbances of all body systems.

Renal failure is classified as acute or chronic.

ACUTE RENAL FAILURE (ARF) Acute renal failure (ARF) usually develops over hours or days with progressive

elevations of blood urea nitrogen (BUN), creatinine, and potassium with or without oliguria. It is a clinical syndrome characterized by a rapid loss of renal function with progressive azotemia.

ARF is often associated with oliguria (a decrease in urinary output to <400 ml/day).

The causes of ARF are multiple and complex. They are categorized according to similar pathogenesis into prerenal (most common), intrarenal (or intrinsic), and postrenal causes.

o Prerenal causes are factors external to the kidneys (e.g., hypovolemia) that reduce renal blood flow and lead to decreased glomerular perfusion and filtration.

o Intrarenal causes include conditions that cause direct damage to the renal tissue, resulting in impaired nephron function. Causes include prolonged ischemia, nephrotoxins, hemoglobin released from hemolyzed RBCs, or myoglobin released from necrotic muscle cells. Acute tubular necrosis (ATN) is an intrarenal condition caused by ischemia, nephrotoxins, or pigments. ATN is potentially reversible if the basement membrane is not destroyed and the tubular epithelium regenerates.

o Postrenal causes involve mechanical obstruction of urinary outflow. Common causes are benign prostatic hyperplasia, prostate cancer, calculi, trauma, and extrarenal tumors.

Clinically, ARF may progress through four phases: initiating, oliguric, diuretic, and recovery. In some situations, the patient does not recover from ARF and chronic kidney disease (CKD) results, eventually requiring dialysis or a kidney transplant.

Oliguric Phase Fluid and electrolyte abnormalities and uremia occur during the oliguric phase. The

kidneys cannot synthesize ammonia or excrete acid products of metabolism, resulting in acidosis.


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Damaged tubules cannot conserve sodium resulting in normal or below-normal levels of serum sodium. Uncontrolled hyponatremia or water excess can lead to cerebral edema. Fluid intake must be closely monitored.

Hyperkalemia is a serious complication of ARF. The serum potassium levels increase because the ability of the kidneys to excrete potassium is impaired. Acidosis worsens hyperkalemia as hydrogen ions enter the cells and potassium is driven out of the cells.

When potassium levels exceed 6 mEq/L (6 mmol/L) or dysrhythmias are identified, treatment must be initiated immediately.

Hematologic disorders associated with ARF include anemia due to impaired erythropoietin production and platelet abnormalities leading to bleeding from multiple sources.

A low serum calcium level results from the inability of the kidneys to activate vitamin D. When hypocalcemia occurs, the parathyroid gland secretes parathyroid hormone, which stimulates bone demineralization, thereby releasing calcium from the bones. Phosphate is also released, leading to elevated serum phosphate levels.

The two most common causes of death in patients with ARF are infection and cardiorespiratory complications.

The best serum indicator of renal failure is creatinine because it is not significantly altered by other factors.

Neurologic changes can occur as the nitrogenous waste products increase. Symptoms can include fatigue and difficulty concentrating, later escalating to seizures, stupor, and coma.

Diuretic Phase The diuretic phase begins with a gradual increase in daily urine output of 1 to 3

L/day, but may reach 3 to 5 L or more. The nephrons are still not fully functional. The uremia may still be severe, as reflected by low creatinine clearances, elevated serum creatinine and BUN levels, and persistent signs and symptoms.

Recovery Phase The recovery phase begins when the GFR increases, allowing the BUN and serum

creatinine levels to plateau and then decrease. Renal function may take up to 12 months to stabilize.

Collaborative Management Because ARF is potentially reversible, the primary goals of treatment are to

eliminate the cause, manage the signs and symptoms, and prevent complications while the kidneys recover.

Common indications for dialysis in ARF are (1) volume overload; (2) elevated potassium level with ECG changes; (3) metabolic acidosis; (4) significant change in mental status; and (5) pericarditis, pericardial effusion, or cardiac tamponade.

Hemodialysis (HD) is used when rapid changes are required in a short period of time. Peritoneal dialysis (PD) is simpler than HD, but it carries the risk of peritonitis, is less efficient in the catabolic patient, and requires longer treatment times. Continuous renal replacement therapy (CRRT) may also be used in the


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treatment of ARF, particularly in those who are hemodynamically unstable.

Prevention of ARF is primarily directed toward identifying and monitoring high-risk populations, controlling exposure to nephrotoxic drugs and industrial chemicals, and preventing prolonged episodes of hypotension and hypovolemia.

The patient with ARF is critically ill and suffers not only from the effects of renal disease but also from the effects of comorbid diseases or conditions (e.g., diabetes, cardiovascular disease).

The nurse has an important role in managing fluid and electrolyte balance during the oliguric and diuretic phases. Observing and recording accurate intake and output and body weight are essential.

Because infection is the leading cause of death in ARF, meticulous aseptic technique is critical. The nurse should be alert for local manifestations of infection (e.g., swelling, redness, pain) as well as systemic manifestations (e.g., malaise, leukocytosis) because an elevated temperature may not be present.

Respiratory complications, especially pneumonitis, can be prevented. Humidified oxygen; incentive spirometry; coughing, turning, and deep breathing; and ambulation are measures to help maintain adequate respiratory ventilation.

Skin care and measures to prevent pressure ulcers should be performed because of edema and decreased muscle tone. Mouth care is important to prevent stomatitis.

Recovery from ARF is highly variable and depends on the underlying illness, the general condition and age of the patient, the length of the oliguric phase, and the severity of nephron damage. Good nutrition, rest, and activity are necessary. Protein and potassium intake should be regulated in accordance with renal function.

The long-term convalescence of 3 to 12 months may cause psychosocial and financial hardships for the family, and appropriate counseling, social work, and psychiatrist/ psychologist referrals are made as needed. If the kidneys do not recover, the patient will eventually need dialysis or transplantation.

Gerontologic Considerations The older adult is more susceptible than the younger adult to ARF as the number

of functioning nephrons decreases with age.

Causes of ARF include dehydration, hypotension, diuretic therapy, aminoglycoside therapy, prostatic hyperplasia, surgery, infection, and radiocontrast agents.

CHRONIC KIDNEY DISEASE Chronic kidney disease (CKD) involves progressive, irreversible loss of kidney

function.

CKD usually develops slowly over months to years and necessitates the initiation of dialysis or transplantation for long-term survival. The prognosis of CKD is variable depending on the etiology, patient’s condition and age, and adequacy of follow-up.

Uremia is a syndrome that incorporates all the signs and symptoms seen in the

various systems throughout the body in CKD.


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In the early stage of renal insufficiency, polyuria results from the inability to concentrate urine. As the GFR decreases, the BUN and serum creatinine levels increase.

Clinical manifestations of uremia develop. Fatigue, lethargy, and pruritus are often the early symptoms. Hypertension and proteinuria are often the first signs. Hyperglycemia, hyperinsulinemia, and abnormal glucose tolerance tests may be seen.

Many patients with uremia develop hyperlipidemia, with elevated very-low-density lipoproteins (VLDLs), normal or decreased low-density lipoproteins (LDLs), and decreased high-density lipoproteins (HDLs).

Hyperkalemia results from the decreased excretion by the kidneys, the breakdown of cellular protein, bleeding, and metabolic acidosis. Potassium may also come from the food consumed, dietary supplements, drugs, and IV infusions.

Because of impaired sodium excretion, sodium along with water is retained resulting in dilutional hyponatremia. Sodium retention can contribute to edema, hypertension, and heart failure.

Metabolic acidosis results from the impaired ability to excrete the acid load (primarily ammonia) and from defective reabsorption and regeneration of bicarbonate.

Normocytic or normochromic anemia is due to decreased production of erythropoietin. The most common cause of bleeding is a qualitative defect in platelet function.

Infectious complications are common in CKD. Clinical findings include lymphopenia, lymphoid tissue atrophy, decreased antibody production, and suppression of the delayed hypersensitivity response.

The most common cardiovascular abnormality is hypertension, which is usually present pre-ESRD and is aggravated by sodium retention and increased extracellular fluid volume. Diabetes mellitus is an additional risk factor.

Cardiac dysrhythmias may result from hyperkalemia, hypocalcemia, and decreased coronary artery perfusion.

Respiratory changes include Kussmaul respiration, dyspnea from fluid overload, pulmonary edema, uremic pleuritis (pleurisy), pleural effusion, and a predisposition to respiratory infections.

Neurologic changes are due to increased nitrogenous waste products, electrolyte imbalances, metabolic acidosis, axonal atrophy, and demyelination. Depression of the CNS results in lethargy, apathy, decreased ability to concentrate, fatigue, irritability, and altered mental ability.

Peripheral neuropathy may result in restless legs syndrome, paresthesias, bilateral footdrop, muscular weakness and atrophy, and loss of deep tendon reflexes.

The treatment for neurologic problems is dialysis or transplantation. Altered mental status is often the signal that dialysis must be initiated.


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Renal osteodystrophy is a syndrome of skeletal changes that is a result of alterations in calcium and phosphate metabolism. Osteomalacia is demineralization resulting from slow bone turnover and defective mineralization of newly formed bone. Osteitis fibrosa cystica results from decalcification of the bone and replacement of bone tissue with fibrous tissue.

Pruritus results from a combination of the dry skin, calcium-phosphate deposition in the skin, and sensory neuropathy.

Both sexes experience infertility and a decreased libido. Sexual dysfunction may also be caused by anemia, peripheral neuropathy, and psychologic problems, physical stress, and side effects of drugs.

Personality and behavioral changes, emotional lability, withdrawal, depression, fatigue, and lethargy are commonly observed. Changes in body image caused by edema, integumentary disturbances, and access devices lead to further anxiety and depression.

Adverse outcomes of CKD can often be prevented or delayed through early detection and treatment. First, conservative therapy is attempted before maintenance dialysis begins. Efforts are made to detect and treat potentially reversible causes of renal failure. The progression of CKD can be delayed by controlling hypertension.

Strategies to reduce serum potassium levels include IV glucose and insulin, IV 10% calcium gluconate, and sodium polystyrene sulfonate (Kayexalate).

The antihypertensive drugs most commonly used are diuretics (e.g., furosemide [Lasix]), -adrenergic blockers (e.g., metoprolol [Lopressor]), calcium channel blockers (e.g., nifedipine [Procardia]), angiotensin-converting enzyme inhibitors (e.g., captopril [Capoten]), and angiotensin receptor blocker agents (e.g., losartan [Cozaar]).

Erythropoietin is used for the treatment of anemia. It can be administered IV or subcutaneously. Statins (HMG-CoA reductase inhibitors) are the most effective drugs for lowering LDL cholesterol levels.

Drug doses and frequency of administration must be adjusted based on the severity of the kidney disease.

Dietary protein is restricted because urea nitrogen and creatinine are end products of protein metabolism. Once the patient starts dialysis, protein intake can be increased. Sufficient calories from carbohydrates and fat are needed to minimize catabolism of body protein and to maintain body weight.

Water intake depends on the daily urine output. Generally, 600 ml (from insensible loss) plus an amount equal to the previous day’s urine output is allowed for a patient who is not receiving dialysis. Phosphate should be limited to approximately 1000 mg/day.

The overall goals are that a patient with CKD will (1) demonstrate knowledge and ability to comply with treatment, (2) participate in decision-making, (3) demonstrate effective coping strategies, and (4) continue with activities of daily living within limitations.


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People at risk for CKD include those with a history (or a family history) of renal disease, hypertension, diabetes mellitus, and repeated urinary tract infection. These individuals should have regular checkups including serum creatinine, BUN, and urinalysis and be advised that any changes in urine appearance, frequency, or volume must be reported to the health care provider.

Dialysis Dialysis is a technique in which substances move from the blood through a

semipermeable membrane and into a dialysis solution (dialysate). The two methods of dialysis are peritoneal dialysis (PD) and hemodialysis (HD).

Peritoneal Dialysis Two types of PD are automated peritoneal dialysis (APD) and continuous

ambulatory peritoneal dialysis (CAPD).o PD is indicated when there are vascular access problems. The three phases

of the PD cycle (called an exchange) are inflow (fill), dwell (equilibration), and drain.

o The patient dialyzing at home will receive about four exchanges per day. Contraindications for PD are history of multiple abdominal surgeries, recurrent abdominal wall or inguinal hernias, excessive obesity with large fat deposits, preexisting vertebral disease, and severe obstructive pulmonary disease.

Dialysis solutions have an electrolyte composition similar to that of plasma. Using dry heat, the dialysis solution is warmed to body temperature to increase peritoneal clearance, prevent hypothermia, and enhance comfort.

CAPD is carried out manually by exchanging 1.5 to 3 L (usually 2 L) of peritoneal dialysate at least 4 times daily, with dwell times of 4 to 10 hours. PD is associated with a short training program, independence, and ease of traveling.

Infection of the peritoneal catheter exit site is most commonly caused by Staphylococcus aureus or S. epidermidis (from skin flora). Peritonitis results from contamination of the dialysate or tubing or from progression of an exit site infection.

Pain is a common complication of PD. A change in the position of the catheter should correct this problem. A decrease in infusion rate may also help. Additional complications include hernias, lower back pain, protein loss, encapsulating sclerosing peritonitis, and bleeding. Atelectasis, pneumonia, and bronchitis may occur from repeated upward displacement of the diaphragm.

Hemodialysis The types of vascular access include arteriovenous fistulas (AVFs) and grafts

(AVGs), temporary and semipermanent catheters, subcutaneous ports, and shunts.

Shunts are not frequently used except for the patient with continuous renal replacement therapy (CRRT) because of the numerous complications (e.g., infection, thrombosis).

An AVF is created most commonly in the forearm with an anastomosis between an artery (usually radial or ulnar) and a vein (usually cephalic). Native fistulas have the best overall patency rates and least number of complications.


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Arteriovenous grafts (AVGs) are made of synthetic materials and form a “bridge” between the arterial and venous blood supplies. Grafts are placed under the skin and are surgically anastomosed between an artery (usually brachial) and a vein (usually antecubital).

BP measurements, insertion of IVs, and venipuncture should never be performed on the affected extremity.

When immediate vascular access is required, percutaneous cannulation of the internal jugular or femoral vein may be performed.

Before beginning treatment, the nurse must complete an assessment that includes fluid status (weight, BP, peripheral edema, lung and heart sounds), condition of vascular access, temperature, and general skin condition.

Hypotension that occurs during HD results from rapid removal of vascular volume, decreased cardiac output, and decreased systemic intravascular resistance. Treatment includes decreasing the volume of fluid being removed and infusion of 0.9% saline solution (100 to 300 ml).

Painful muscle cramps due to rapid removal of sodium and water are a common problem. Treatment includes reducing the ultrafiltration rate and infusing hypertonic saline or a normal saline bolus.

The causes of hepatitis B and C (most common) in dialysis patients include blood transfusions or the lack of adherence to precautions used to prevent the spread of infection.

Disequilibrium syndrome develops as a result of very rapid changes in the composition of the extracellular fluid. Manifestations include nausea, vomiting, confusion, restlessness, headaches, twitching and jerking, and seizures.

Individual adaptation to maintenance HD varies considerably. The primary nursing goals are to help the patient regain or maintain positive self-esteem and control of his or her life and to continue to be productive in society.

Continuous Renal Replacement Therapy Continuous renal replacement therapy (CRRT) is an alternative or adjunctive

treatment.

Uremic toxins and fluids are removed, while acid-base status and electrolytes are adjusted slowly and continuously from a hemodynamically unstable patient.

Vascular access is achieved through the use of a double-lumen catheter placed in

the femoral, jugular, or subclavian vein. Anticoagulation is used to prevent blood clotting during CRRT.

Kidney Transplantation One-year graft survival rates for kidney transplantation are 90% for deceased

donor transplants and 95% for live donor transplants.

Contraindications to transplantation include disseminated malignancies, refractory or untreated cardiac disease, chronic respiratory failure, extensive vascular disease, chronic infection, and unresolved psychosocial disorders.


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Kidneys for transplantation may be obtained from compatible-blood-type deceased donors, blood relatives, emotionally related living donors, and altruistic living donors.

Live donors must undergo an extensive evaluation to be certain that they are in good health and have no history of disease that would place them at risk for developing kidney failure or operative complications.

Deceased (cadaver) kidney donors are relatively healthy individuals who have suffered an irreversible brain injury. Permission from the donor’s legal next of kin is required after brain death is determined even if the donor carried a signed donor card.

For a live donor transplant, the donor nephrectomy is performed either through an open incision or laparoscopically. The short cold ischemic time is the primary reason for the success of living donor transplants.

The transplanted kidney is usually placed extraperitoneally in the right iliac fossa to facilitate anastomoses and minimize the occurrence of ileus. Nursing care of the patient in the preoperative phase includes emotional and physical preparation for surgery.

The usual postoperative care for the living donor is similar to that following conventional or laparoscopic nephrectomy.

For the kidney transplant recipient the first priority during this period is maintenance of fluid and electrolyte balance. Very large volumes of urine may be produced soon after the blood supply to the transplanted kidney is reestablished. This is due to (1) the new kidney’s ability to filter BUN, which acts as an osmotic diuretic; (2) the abundance of fluids administered during the operation; and (3) initial renal tubular dysfunction, which inhibits the kidney from concentrating urine normally.

Postoperative teaching should include the prevention and treatment of rejection, infection, and complications of surgery and the purpose and side effects of immunosuppression.

Rejection, a major problem following kidney transplantation, can be hyperacute, acute, or chronic. Immunosuppressive therapy is used to prevent rejection while maintaining sufficient immunity to prevent overwhelming infection.

Infection is a significant cause of morbidity and mortality after kidney transplantation. Transplant recipients usually receive prophylactic antifungal drugs. Viral infections can be primary or reactivation of existing disease. CMV is one of the most common viral infections.

Cardiovascular disease is the leading cause of death after renal transplantation. Hypertension, hyperlipidemia, diabetes mellitus, smoking, rejection, infections, and increased homocysteine levels can all contribute to cardiovascular disease.

The overall incidence of malignancies in kidney transplant recipients is 100 times greater than in the general population. The primary cause is the immunosuppressive therapy.

Aseptic necrosis of the hips, knees, and other joints can result from chronic


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corticosteroid therapy and renal osteodystrophy.

Gerontologic Considerations Approximately 35% to 65% of patients who have CKD are 65 or older. Physiologic

changes in the older CKD patient include diminished cardiopulmonary function, bone loss, immunodeficiency, altered protein synthesis, impaired cognition, and altered drug metabolism.

Most elderly ESRD patients select home dialysis. However, establishing vascular access for HD may be challenging due to atherosclerotic changes.

The most common cause of death in the elderly ESRD patient is cardiovascular disease (MI, stroke), followed by withdrawal from dialysis.


Key Points

Chapter 48: Nursing Assessment: Endocrine System

STRUCTURES AND FUNCTIONS Hormones exert their effects on target tissue.

The specificity of hormone–target cell interaction is determined by receptors in a “lock-and-key” type of mechanism.

The regulation of hormone levels in the blood depends on a highly specialized mechanism called feedback.

With negative feedback, the gland responds by increasing or decreasing the secretion of a hormone based on feedback from various factors.

The hypothalamus and pituitary gland integrate communication between the nervous and endocrine systems.

Anterior Pituitary Several hormones secreted by the anterior pituitary are referred to as tropic

hormones because they control the secretion of hormones by other glands. o Thyroid-stimulating hormone (TSH) stimulates the thyroid gland to secrete

thyroid hormones. o Adrenocorticotropic hormone (ACTH) stimulates the adrenal cortex to secrete

corticosteroids. o Follicle-stimulating hormone (FSH) stimulates secretion of estrogen and the

development of ova in the female and sperm development in the male. o Luteinizing hormone (LH) stimulates ovulation in the female and secretion of

sex hormones in both the male and female.

Growth hormone (GH) has effects on all body tissues.

Antidiuretic hormone (ADH) regulates fluid volume by stimulating reabsorption of water in the kidneys.

Oxytocin stimulates ejection of milk into mammary ducts and contraction of uterine smooth muscle.


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Thyroid Gland The major function of the thyroid gland is the production, storage, and release of

the thyroid hormones, thyroxine (T4) and triiodothyronine (T3).o Iodine is necessary for the synthesis of thyroid hormones.o T4 and T3 affect metabolic rate, carbohydrate and lipid metabolism, growth and

development, and nervous system activities.

Calcitonin is a hormone produced by C cells (parafollicular cells) of the thyroid gland in response to high circulating calcium levels.

Parathyroid Gland The parathyroid glands are four small, oval structures usually arranged in pairs

behind each thyroid lobe. They secrete parathyroid hormone (PTH), which regulates the blood level of calcium.

Adrenal Gland The adrenal glands are small, paired, highly vascularized glands located on the

upper portion of each kidney. o The adrenal medulla secretes the catecholamines epinephrine (the major

hormone [75%]), norepinephrine (25%), and dopamine. o The adrenal cortex secretes cortisol, which is the most abundant and potent

glucocorticoid. Cortisol is necessary to maintain life. Its functions include regulation of blood glucose concentration, inhibition of inflammatory action, and support in response to stress.

o Aldosterone is a potent mineralocorticoid that maintains extracellular fluid volume.

o The adrenal cortex secretes small amounts of androgens. Adrenal androgens stimulate pubic and axillary hair growth and sex drive in females.

Pancreas The pancreas secretes several hormones, including glucagon and insulin. o Glucagon increases blood glucose by stimulating glycogenolysis,

gluconeogenesis, and ketogenesis.o Insulin is the principal regulator of the metabolism and storage of ingested

carbohydrates, fats, and proteins.

Gerontologic Considerations Normal aging results in decreased hormone production and secretion, altered

hormone metabolism and biologic activity, decreased responsiveness of target tissues to hormones, and alterations in circadian rhythms.

Subtle changes of aging often mimic manifestations of endocrine disorders.

ASSESSMENT Hormones affect every body tissue and system, causing great diversity in the signs

and symptoms of endocrine dysfunction.

Endocrine dysfunction may result from deficient or excessive hormone secretion, transport abnormalities, an inability of the target tissue to respond to a hormone, or inappropriate stimulation of the target-tissue receptor.

Subjective data:o The nurse should inquire about use of hormone replacements, previous

hospitalizations, surgery, chemotherapy, and radiation therapy (especially of the neck).


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Objective data:o Most endocrine glands are inaccessible to direct examination.

Physical examination:o Clinical manifestations of endocrine function vary significantly, depending on

the gland involved.o Assessment includes a history of growth and development, weight distribution

and changes, and comparisons of these factors with normal findings.o Disorders can commonly cause changes in mental and emotional status.o The nurse should note the color and texture of the skin, hair, and nails. The skin

should be palpated for skin texture and presence of moisture.o When inspecting the thyroid gland, observation should be made first in the

normal position (preferably with side lighting), then in slight extension, and then as the patient swallows some water.

o The thyroid is palpated for its size, shape, symmetry, and tenderness and for any nodules.

o The size, shape, symmetry, and general proportion of hand and feet size should be assessed.

o The hair distribution pattern of the genitalia should be inspected.

DIAGNOSTIC STUDIES Laboratory tests usually involve blood and urine testing.

Ultrasound may be used as a screening tool to localize endocrine growths such as thyroid nodules.

Laboratory studies may include direct measurement of the hormone level, or involve an indirect indication of gland function by evaluating blood or urine components affected by the hormone (e.g., electrolytes).

Notation of sample time on the laboratory slip and sample is important for hormones with circadian or sleep-related secretion.

The studies used to assess function of the anterior pituitary hormones relate to GH, prolactin, FSH, LH, TSH, and ACTH.

Tests to assess abnormal thyroid function include TSH (most common), total T4, free T4, and total T3.


Key Points

Chapter 49: Nursing Management: Diabetes Mellitus

Diabetes mellitus is a chronic multisystem disorder of glucose metabolism related to absent or insufficient insulin supplies and/or poor utilization of the insulin that is available.

The two most common types of diabetes are classified as type 1 or type 2 diabetes mellitus. Gestational diabetes, prediabetes, and secondary diabetes are other classifications of diabetes commonly seen in clinical practice.


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1 TYPE 1 DIABETES

Type 1 diabetes mellitus most often occurs in people who are under 30 years of age, with a peak onset between ages 11 and 13, but can occur at any age.

Type 1 diabetes is the end result of a long-standing process where the body’s own T cells attack and destroy pancreatic beta cells, which are the source of the body’s insulin.

Because the onset of type 1 diabetes is rapid, the initial manifestations are usually acute. The classic symptoms are polyuria, polydipsia, and polyphagia.

The individual with type 1 diabetes requires a supply of insulin from an outside source (exogenous insulin), such as an injection, in order to sustain life. Without insulin, the patient will develop diabetic ketoacidosis (DKA), a life-threatening condition resulting in metabolic acidosis.

1.1 PREDIABETES

Prediabetes is a condition where blood glucose levels are higher than normal but not high enough for a diagnosis of diabetes. Most people with prediabetes are at increased risk for developing type 2 diabetes and if no preventive measures are taken, they will usually develop it within 10 years.

Long-term damage to the body, especially the heart and blood vessels, may already be occurring in patients with prediabetes.

1.2 TYPE 2 DIABETES

Type 2 diabetes mellitus is, by far, the most prevalent type of diabetes, accounting for over 90% of patients with diabetes.

In type 2 diabetes, the pancreas usually continues to produce some endogenous (self-made) insulin. However, the insulin that is produced is either insufficient for the needs of the body and/or is poorly used by the tissues.

The most important risk factors for developing type 2 diabetes are believed to be obesity, specifically abdominal and visceral adiposity. Also, individuals with metabolic syndrome are at an increased risk for the development of type 2 diabetes.

Some of the more common manifestations associated with type 2 diabetes include fatigue, recurrent infections, recurrent vaginal yeast or monilia infections, prolonged wound healing, and visual changes.

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1.4 GESTATIONAL DIABETES

Gestational diabetes develops during pregnancy and is detected at 24 to 28 weeks of gestation, usually following an oral glucose tolerance test.

Although most women with gestational diabetes will have normal glucose levels within 6 weeks postpartum, their risk for developing type 2 diabetes in 5 to 10 years is increased.


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A diagnosis of diabetes is based on one of three methods: (1) fasting plasma glucose level, (2) random plasma glucose measurement, or (3) 2-hour oral glucose tolerance test.

The goals of diabetes management are to reduce symptoms, promote well-being, prevent acute complications of hyperglycemia, and prevent or delay the onset and progression of long-term complications. These goals are most likely to be met when the patient is able to maintain blood glucose levels as near to normal as possible.

2 INSULIN THERAPY

Exogenous (injected) insulin is needed when a patient has inadequate insulin to meet specific metabolic needs.

Insulin is divided into two main categories: short-acting (bolus) and long-acting (basal) insulin. Basal insulin is used to maintain a background level of insulin throughout the day and bolus insulin is used at mealtime.

A variety of insulin regimens are recommended for patients depending on the needs of the patient and their preference.

Routine administration of insulin is most commonly done by means of subcutaneous injection, although intravenous administration of regular insulin can be done when immediate onset of action is desired.

The technique for insulin injections should be taught to new insulin users and reviewed periodically with long-term users.

The speed with which peak serum concentrations are reached varies with the anatomic site for injection. The fastest absorption is from the abdomen.

Continuous subcutaneous insulin infusion can be administered using an insulin pump, a small battery-operated device that resembles a standard paging device in size and appearance. The device is programmed to deliver a continuous infusion of rapid-acting or short-acting insulin 24 hours a day and at mealtime, the user programs the pump to deliver a bolus infusion of insulin.

An alternative to injectable insulin is inhaled insulin. Exubera is a rapid-acting, dry powder form of insulin that is inhaled through the mouth into the lungs prior to eating via a specially designed inhaler.

Hypoglycemia, allergic reactions, lipodystrophy, and the Somogyi effect are problems associated with insulin therapy.

o Lipodystrophy (atrophy of subcutaneous tissue) may occur if the same injection sites are used frequently.

o The Somogyi effect is a rebound effect in which an overdose of insulin induces hypoglycemia. Usually occurring during the hours of sleep, the Somogyi effect produces a decline in blood glucose level in response to too much insulin.

o The dawn phenomenon is characterized by hyperglycemia that is present on awakening in the morning due to the release of counterregulatory hormones in the predawn hours.


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3

4 ORAL AGENTS

Oral agents (OAs) are not insulin, but they work to improve the mechanisms by which insulin and glucose are produced and used by the body. OAs work on the three defects of type 2 diabetes, including (1) insulin resistance, (2) decreased insulin production, and (3) increased hepatic glucose production.

Sulfonylureas are frequently the drugs of choice in treating type 2 diabetes due to the decreased chance of prolonged hypoglycemia. The primary action of the sulfonylureas is to increase insulin production from the pancreas.

Like the sulfonylureas, meglitinides increase insulin production from the pancreas. But because they are more rapidly absorbed and eliminated, they offer a reduced potential for hypoglycemia.

Metformin (Glucophage) is a biguanide glucose-lowering agent. The primary action of metformin is to reduce glucose production by the liver.

α-Glucosidase inhibitors, also known as “starch blockers,” these drugs work by slowing down the absorption of carbohydrate in the small intestine.

Sometimes referred to as “insulin sensitizers,” thiazolidinediones are most effective for people who have insulin resistance. They improve insulin sensitivity, transport, and utilization at target tissues.

OTHER DRUG THERAPIES Pramlintide (Symlin) is a synthetic analog of human amylin, a hormone secreted by the β cells of the pancreas. When taken concurrently with insulin, it provides for better glucose control.

Exanatide (Byetta) is a synthetic peptide that stimulates the release of insulin from the pancreatic β cells. Exanatide is administered using a subcutaneous injection.

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6 NUTRITIONAL THERAPY AND EXERCISE

The overall goal of nutritional therapy is to assist people with diabetes in making healthy nutritional choices, eating a varied diet, and maintaining exercise habits that will lead to improved metabolic control.

For those with type 1 diabetes, day-to-day consistency in timing and amount of food eaten is important for those individuals using conventional, fixed insulin regimens. Patients using rapid-acting insulin can make adjustments in dosage before the meal based on the current blood glucose level and the carbohydrate content of the meal.

The emphasis for nutritional therapy in type 2 diabetes should be placed on achieving glucose, lipid, and blood pressure goals.

The nutritional energy intake should be constantly balanced with the energy output of the individual, taking into account exercise and metabolic body work.

In a general diabetic meal plan, carbohydrates and monounsaturated fat should provide 45% to 65% of the total energy intake each day. Fats should compose no more than 25% to 30% of the meal plan’s total calories, with less than 7% of calories


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from saturated fats, and protein should contribute less than 10% of the total energy consumed.

Alcohol is high in calories, has no nutritive value, and promotes hypertriglyceridemia. Patients should be cautioned to honestly discuss the use of alcohol with their health care providers because its use can make blood glucose more difficult to control.

Regular, consistent exercise is considered an essential part of diabetes and prediabetes management. Exercise increases insulin receptor sites in the tissue and can have a direct effect on lowering the blood glucose levels.

7 MONITORING BLOOD GLUCOSE

Self-monitoring of blood glucose (SMBG) is a cornerstone of diabetes management. By providing a current blood glucose reading, SMBG enables the patient to make self-management decisions regarding diet, exercise, and medication.

The frequency of monitoring depends on several factors, including the patient’s glycemic goals, the type of diabetes that the patient has, the patient’s ability to perform the test independently, and the patient’s willingness to test.

8 PANCREAS TRANSPLANTATION

Pancreas transplantation can be used as a treatment option for patients with type 1 diabetes mellitus. Most commonly it is done for patients who have end-stage renal disease and who have had or plan to have a kidney transplant.

Kidney and pancreas transplants are often performed together, or a pancreas may be transplanted following a kidney transplant. Pancreas transplants alone are rare.

9 NURSING MANAGEMENT

Nursing responsibilities for the patient receiving insulin include proper administration, assessment of the patient’s response to insulin therapy, and education of the patient regarding administration, adjustment to, and side effects of insulin.

Proper administration, assessment of the patient’s use of and response to the OA, and education of the patient and the family about OAs are all part of the nurse’s function.

The goals of diabetes self-management education are to enable the patient to become the most active participant in his or her care, while matching the level of self-management to the ability of the individual patient.

10 ACUTE COMPLICATIONS OF DIABETES MELLITUS

Diabetic ketoacidosis (DKA), also referred to as diabetic acidosis and diabetic coma, is caused by a profound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, and dehydration. It is most likely to occur in people with type 1 diabetes.

o DKA is a serious condition that proceeds rapidly and must be treated promptly.


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o Because fluid imbalance is potentially life threatening, the initial goal of therapy is to establish intravenous access and begin fluid and electrolyte replacement.

Hyperosmolar hyperglycemic syndrome (HHS) is a life-threatening syndrome that can occur in the patient with diabetes who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion.

Hypoglycemia, or low blood glucose, occurs when there is too much insulin in proportion to available glucose in the blood. Causes of hypoglycemia are often related to a mismatch in the timing of food intake and the peak action of insulin or oral hypoglycemic agents that increase endogenous insulin secretion.

11 CHRONIC COMPLICATIONS OF DIABETES MELLITUS

Chronic complications of diabetes are primarily those of end-organ disease from damage to blood vessels secondary to chronic hyperglycemia. These chronic blood vessel dysfunctions are divided into two categories: macrovascular complications and microvascular complications.

o Macrovascular complications are diseases of the large and medium-sized blood vessels that occur with greater frequency and with an earlier onset in people with diabetes.

o Microvascular complications result from thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia.

Diabetic retinopathy refers to the process of microvascular damage to the retina as a result of chronic hyperglycemia in patients with diabetes.

Diabetic nephropathy is a microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney.

Diabetic neuropathy is nerve damage that occurs because of the metabolic derangements associated with diabetes mellitus. The two major categories of diabetic neuropathy are sensory neuropathy, which affects the peripheral nervous system, and autonomic neuropathy.

o The most common form of sensory neuropathy is distal symmetric neuropathy, which affects the hands and/or feet bilaterally. This is sometimes referred to as “stocking-glove neuropathy.”

o Autonomic neuropathy can affect nearly all body systems and lead to hypoglycemic unawareness, bowel incontinence and diarrhea, and urinary retention.

12 Complications of the Feet and Lower Extremities

Foot complications are the most common cause of hospitalization in the person with diabetes.

Sensory neuropathy is a major risk factor for lower extremity amputation in the person with diabetes. Loss of protective sensation often prevents the patient from becoming aware that a foot injury has occurred.

Proper care of a diabetic foot ulcer is critical to prevention of infections.


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Key Points

Chapter 50: Nursing Management: Endocrine Problems

13 ACROMEGALY

Acromegaly results from excess secretion of growth hormone (GH).

It is a rare condition of bone and soft tissue overgrowth.

Bones increase in thickness and width but not length.

Manifestations include enlargement of hands and feet, thickening and enlargement of face and head bony and soft tissue, sleep apnea, signs of diabetes mellitus, cardiomegaly, and hypertension.

Treatment focuses on returning GH levels to normal through surgery, radiation, and drug therapy. The prognosis depends on age at onset, age when treatment is initiated, and tumor size.

Nursing care for surgical patients postoperatively includes avoidance of vigorous coughing, sneezing, and straining at stool to prevent cerebrospinal fluid leakage from where the sella turcica was entered.

After surgery with a transsphenoidal approach, the head of the bed is elevated to a 30-degree angle at all times, and neurologic status is monitored. Mild analgesia is used for headaches, and toothbrushing is avoided for at least 10 days.

If hypophysectomy is done or the pituitary is damaged, antidiuretic hormone (ADH), cortisol, and thyroid hormone replacement must be taken for life. Patient teaching is essential with hormone replacement therapy.

HYPOPITUITARISM Hypopituitarism is rare, and involves a decrease in one or more of the pituitary

hormones:o The anterior pituitary gland secretes adrenocorticotrophic hormone

(ACTH), thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), GH, and prolactin.

o The posterior pituitary gland secretes ADH and oxytocin.

Most deficiencies associated with hypopituitarism involve GH and gonadotropins (e.g., LH, FSH) due to a pituitary tumor.

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE Syndrome of inappropriate antidiuretic hormone (SIADH) results from an

overproduction or oversecretion of ADH.

SIADH results from abnormal production or sustained secretion of ADH and is characterized by fluid retention, serum hypoosmolality, dilutional hyponatremia, hypochloremia, concentrated urine in presence of normal or increased intravascular volume, and normal renal function.


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The most common cause is lung cancer.

Treatment is directed at underlying cause, with a goal to restore normal fluid volume and osmolality. Fluid restriction results in gradual, daily weight reductions, progressive rise in serum sodium concentration and osmolality, and symptomatic improvement. With chronic SIADH, the patient must learn self-management.

DIABETES INSIPIDUS Diabetes insipidus (DI) is associated with deficiency of production or

secretion of ADH or decreased renal response to ADH.

Decreases in ADH cause fluid and electrolyte imbalances due to increased urinary output and increased plasma osmolality.

Depending on the cause, DI may be transient or chronic lifelong condition.

Types of DI include:o Central DI (or neurogenic DI) occurs when an organic lesion of the

hypothalamus, infundibular stem, or posterior pituitary interferes with ADH synthesis, transport, or release.

o Nephrogenic DI occurs when there is adequate ADH, but a decreased kidney response to ADH. Lithium is a common cause of drug-induced nephrogenic DI. Hypokalemia and hypercalcemia may also lead to nephrogenic DI.

o Psychogenic DI is associated with excessive water intake, caused by lesion in thirst center or by psychosis.

DI is characterized by polydipsia and polyuria.

If oral fluid intake cannot keep up with urinary losses, severe fluid volume deficit results as manifested by weight loss, constipation, poor tissue turgor, hypotension, and shock.

Severe dehydration and hypovolemic shock may occur.

Treating the primary cause is central to management. Therapeutic goal is maintenance of fluid and electrolyte balance.

Nursing care includes early detection, maintenance of adequate hydration, and patient teaching for long-term management.

GOITER Goiter is thyroid gland hypertrophy and enlargement caused by excess TSH

stimulation, which can be caused by inadequate circulating thyroid hormones.

Goiter is also found in Graves’ disease.

TSH and T4 levels are measured to determine if goiter is associated with hyperthyroidism, hypothyroidism, or normal thyroid function.

Thyroid antibodies are measured to assess for thyroiditis.

Treatment with thyroid hormone may prevent further thyroid enlargement.

Surgery to remove large goiters may be done.


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THYROID NODULES A thyroid nodule, a palpable deformity of the thyroid gland, may be benign or

malignant.

Benign nodules are usually not dangerous, but can cause tracheal compression if they become too large.

Malignant tumors of thyroid gland are rare.

A major sign of thyroid cancer is presence of hard, painless nodule or nodules on enlarged thyroid gland.

Surgical tumor removal is usually indicated with cancer.

Procedures include unilateral total lobectomy with removal of isthmus to total thyroidectomy with bilateral lobectomy.

Radiation therapy may also be indicated.

Nursing care for thyroid tumors is similar to care for patient who has undergone thyroidectomy.

THYROIDITIS Thyroiditis is an inflammatory process in the thyroid gland.

Subacute and acute forms of thyroiditis have abrupt onset, and the thyroid gland is painful.

Chronic autoimmune thyroiditis (Hashimoto’s thyroiditis) can lead to hypothyroidism.

Hashimoto’s thyroiditis is a chronic autoimmune disease in which thyroid tissue is replaced by lymphocytes and fibrous tissue. It is most common cause of goiterous hypothyroidism.

Recovery may be complete in weeks or months without treatment.

HYPERTHYROIDISM Hyperthyroidism is thyroid gland hyperactivity with sustained increase in synthesis

and release of thyroid hormones.

Thyrotoxicosis refers to physiologic effects or clinical syndrome of hypermetabolism resulting from excess circulating levels of T4, T3, or both.

Hyperthyroidism and thyrotoxicosis usually occur together as in Graves’ disease.

The most common form of hyperthyroidism is Graves’ disease.

Other causes include toxic nodular goiter, thyroiditis, exogenous iodine excess, pituitary tumors, and thyroid cancer.

Graves’ Disease Graves’ disease is an autoimmune disease marked by diffuse thyroid enlargement

and excessive thyroid hormone secretion.


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Factors such as insufficient iodine supply, infection, and stressful life events may interact with genetic factors to cause Graves’ disease.

Manifestations relate to the effect of thyroid hormone excess.

When thyroid gland is large, a goiter may be noted, and auscultation of thyroid gland may reveal bruits.

A classic finding is exophthalmos, a protrusion of eyeballs from the orbits.

Treatment options are antithyroid medications, radioactive iodine therapy, and subtotal thyroidectomy.

Thyrotoxic Crisis Thyrotoxic crisis, also known as thyroid storm, is an acute, rare condition in which

all hyperthyroid manifestations are heightened.

Although it is a life-threatening emergency, death is rare when treatment is vigorous and initiated early.

Manifestations include severe tachycardia, shock, hyperthermia, seizures, abdominal pain, diarrhea, delirium, and coma.

Treatment focuses on reducing circulating thyroid hormone levels by drug therapy.

HYPOTHYROIDISM Hypothyroidism is one of most common medical disorders.

It results from insufficient circulating thyroid hormone.

This condition may be primary (related to destruction of thyroid tissue or defective hormone synthesis), or secondary (related to pituitary disease with decreased TSH secretion or hypothalamic dysfunction with decreased thyrotropin-releasing hormone [TRH] secretion).

Hypothyroidism also can be transient and related to thyroiditis or from a discontinuation of thyroid hormone therapy.

Iodine deficiency is the most common cause worldwide.

In areas with adequate iodine intake, the most common cause is thyroid gland atrophy (end result of Hashimoto’s thyroiditis and Graves’ disease).

Manifestations include fatigue, lethargy, personality and mental changes, decreased cardiac output, anemia, and constipation.

Patients with severe long-standing hypothyroidism may display myxedema, an accumulation of hydrophilic mucopolysaccharides in dermis and other tissues. This mucinous edema causes characteristic facies of hypothyroidism (i.e., puffiness, periorbital edema, and masklike affect).

A myxedema coma can be precipitated by infection, drugs (especially opioids, tranquilizers, and barbiturates), exposure to cold, and trauma. This condition is characterized by subnormal temperature, hypotension, and hypoventilation. To


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survive, vital functions are supported and IV thyroid hormone replacement administered.

The overall treatment in hypothyroidism is restoration of euthyroid state as safely and rapidly as possible with hormone replacement therapy.

Levothyroxine (Synthroid) is the drug of choice.

Patient teaching is imperative, and the need for lifelong drug therapy is stressed.

HYPERPARATHYROIDISM Hyperparathyroidism involves increased secretion of parathyroid hormone (PTH).

Excess PTH leads to hypercalcemia and hypophosphatemia.

Manifestations include weakness, loss of appetite, constipation, emotional disorders, and shortened attention span.

Major signs include osteoporosis, fractures, and kidney stones.

Neuromuscular abnormalities are muscle weakness in proximal muscles of lower extremities.

Parathyroidectomy leads to a reduction in chronically high calcium levels.

Continued ambulation, avoidance of immobility, a high fluid intake and moderate calcium intake are important.

Several drugs are helpful in lowering calcium levels: bisphosphonates (e.g., alendronate [Fosamax]) estrogen or progestin therapy, oral phosphate, diuretics, and calcimimetic agents (e.g., cinacalcet [Sensipar]).

HYPOPARATHYROIDISM Hypoparathyroidism is rare, and results from inadequate circulating PTH.

It is characterized by hypocalcemia resulting from a lack of PTH to maintain serum calcium levels.

The most common cause is iatrogenic, due to accidental removal of parathyroid glands or damage to these glands during neck surgery.

Sudden decreases in serum calcium cause tetany, which is characterized by tingling of lips, fingertips, and increased muscle tension with paresthesias and stiffness.

Painful tonic spasms of smooth and skeletal muscles (extremities and face), and laryngospasms and a positive Chvostek sign and Trousseau sign are usually present.

Focus of patient care is to treat tetany, maintain normal serum calcium levels, and prevent long-term complications. Emergency treatment of tetany requires IV calcium.

Instruction about lifelong treatment and follow-up care includes monitoring of calcium levels.

CUSHING SYNDROME


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Cushing syndrome is a spectrum of clinical abnormalities caused by excessive corticosteroids, particularly glucocorticoids.

The most common cause is iatrogenic administration of exogenous corticosteroids (e.g., prednisone).

Most cases of endogenous Cushing syndrome are due to adrenocorticotrophic hormone (ACTH) secreting pituitary tumor (Cushing’s disease).

Key signs include centripedal or generalized obesity, “moon facies” (fullness of face), purplish red striae below the skin surface, hirsutism in women, hypertension, and unexplained hypokalemia.

Treatment is dependent on the underlying cause, and includes surgery and drug therapy to normalize hormone levels.

Discharge instructions are based on patient’s lack of endogenous corticosteroids and resulting inability to react to stressors physiologically.

Lifetime replacement therapy is required by many patients.

ADDISON’S DISEASE In the patient with Addison’s disease, all three classes of adrenal corticosteroids

(glucocorticoids, mineralocorticoids, and androgens) are reduced.

The etiology is mostly autoimmune where adrenal cortex is destroyed by autoantibodies.

Manifestations have a slow onset and include weakness, weight loss, and anorexia.

Skin hyperpigmentation is seen in sun-exposed areas of body, at pressure points, over joints, and in palmar creases.

The treatment is replacement therapy. Hydrocortisone, the most commonly used form of replacement therapy, has both glucocorticoid and mineralocorticoid properties. During times of stress, glucocorticoid dosage is increased to prevent addisonian crisis.

Mineralocorticoid replacement with fludrocortisone acetate (Florinef) is given daily with increased dietary salt. Patient teaching covers medications, techniques for stress management, and that patient must always wear an identification bracelet (Medic Alert).

Addisonian Crisis Patients with Addison’s disease are at risk for an acute adrenal insufficiency

(addisonian crisis), a life-threatening emergency caused by insufficient or sudden decrease in adrenocortical hormones.

Addisonian crisis is triggered by stress (e.g., surgery, trauma, hemorrhage, or psychologic distress); sudden withdrawal of corticosteroid hormone replacement therapy; and post-adrenal surgery.

Manifestations include postural hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, and confusion.


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Treatment is shock management and high-dose hydrocortisone replacement. Large volumes of 0.9% saline solution and 5% dextrose are given to reverse hypotension and electrolyte imbalances until blood pressure normalizes.

LONG-TERM ADMINISTRATION OF CORTICOSTEROIDS The use of long-term corticosteroids in therapeutic doses often leads to serious

complications and side effects.

Therapy is reserved for diseases in which there is a risk of death or permanent loss of function, and conditions in which short-term therapy is likely to produce remission or recovery.

The potential treatment benefits must always be weighed against risks.

The danger of abrupt cessation of corticosteroid therapy must be emphasized to patients and significant others.

Corticosteroids taken longer than 1 week will suppress adrenal production and oral corticosteroids should be tapered.

Nurses must ensure that increased doses of corticosteroids are prescribed in acute care or home care situations with increased physical or emotional stress.

HYPERALDOSTERONISM Hyperaldosteronism is characterized by excessive aldosterone secretion commonly

caused by small solitary adrenocortical adenoma.

The main effects are sodium retention and potassium and hydrogen ion excretion.

A key sign of this disease is hypertension with hypokalemic alkalosis.

The preferred treatment is surgical removal of adenoma (adrenalectomy).

Patients with bilateral adrenal hyperplasia are treated with drugs. Calcium channel blockers may be used to control BP.

Patients are taught to monitor own BP and need for monitoring.

PHEOCHROMOCYTOMA Pheochromocytoma is a rare condition characterized by an adrenal medulla tumor

that produces excessive catecholamines (epinephrine, norepinephrine).

The tumor is benign in most cases.

The secretion of excessive catecholamines results in severe hypertension.

If undiagnosed and untreated, pheochromocytoma may lead to diabetes mellitus, cardiomyopathy, and death.

Manifestations include severe, episodic hypertension accompanied by classic triad of (1) severe, pounding headache, (2) tachycardia with palpitations and profuse sweating, and (3) unexplained abdominal or chest pain.

Attacks may be provoked by many medications, including antihypertensives, opioids, radiologic contrast media, and tricyclic antidepressants.


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The treatment consists of surgical removal of tumor.


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Documents

2nd Med Surg Exam Key Points